Prolonged neonatal phosphate retention and transient hypercalcemia following antenatal Burosumab exposure: a pharmacovigilance alert.

Burosumab is a monoclonal antibody targeting fibroblast growth factor 23 (FGF23) and is approved for the treatment of X-linked hypophosphatemia. Its use during pregnancy has not been studied, and fetal exposure may affect neonatal mineral metabolism. We report a neonate exposed to Burosumab throughout gestation who developed prolonged phosphate retention, suppressed parathyroid hormone, and transient hypercalcemia after birth. Serial biochemical monitoring demonstrated persistently elevated tubular phosphate reabsorption and low urinary phosphate excretion beyond the early neonatal period, consistent with sustained pharmacodynamic effects of FGF23 inhibition. These abnormalities gradually resolved over time, and the infant remained clinically well with normal growth and no evidence of nephrocalcinosis. Genetic testing excluded the familial pathogenic PHEX variant, confirming that the observed phenotype was due to transient pharmacologic exposure rather than intrinsic disease. This case demonstrates that antenatal Burosumab exposure can result in prolonged postnatal alterations in calcium-phosphate homeostasis. Careful biochemical monitoring is warranted in exposed infants, and continuation of Burosumab beyond mid-pregnancy should be approached with caution.